Factors

We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions.
o

Tec1 is a positive regulator of chronological lifespan. Absence of TEC1 causes a significant shortened chronological lifespan, but does not block chronological lifespan extension by rapamycin. TEC(AxY) mutation also reduces chronological lifespan, although not so pronounced as strains lacking TEC1. Rapamycin-induced chronological lifespan extension is almost completely blocked by TEC(AxY) allele [21840851].

Deletion of ATH1 extend the mean chronological lifespan by 17% (at 30 degree Celsus in BY4742) [22783207].
ATH1 mutants have higher trehalose levels until the end of the post-diauxic growth phase, but reaches a plateau at the level of 50-70% of wild-type in the stationary phase [22783207].

Deletion of TPS3 extend the mean chronological lifespan by 39% (at 30 degree Celsus in BY4742) [22783207].
TPS3 mutants have higher trehalose levels until the end of the post-diauxic growth phase, but reaches a plateau at the level of 50-70% of wild-type in the stationary phase [22783207].

esa1-531 mutant has an even shorter chronological lifespan than PKA1 deletion mutant in both 2% glucose (ad libitum) and water (extreme DR) at 30 degree Celsius, a semipermissive temperature. At the permissive temperature (25 degree Celsius) there is little difference [19303850].

ACH1 deletion cells accumulate a high amount of extracellular acetic acid and display a reduced mean and maximum chronological lifespan. Maximum lifespan is reduced by 32%. Lifespan shortening is completely abrogated by alleviating the acid stress either by a DR regimen that prevents acetic acid production or by transferring chronologically aging mutant cells to water. Deletion of ACH1 is accompanied by reactive oxygen species accumulation, severe mitochondrial damage, and an early insurgence of apoptosis [22754872].

Deletion of TPS2 has no effect on replicative lifespan and does not prevent lifespan extension by high osmolarity [12391171].
TPS2 is required for trehalose biosynthesis in response to osmotic stress [8444170].

Deletion of SWI4 shortens replicative lifespan by approximately 90% [11805047]. SSD1-V partially suppresses the short lifespan of a swi4 mutant.
Mutation of swi4 results in slow growth and temperature sensitivity, both of which are suppressed by SSD1-V [11805047].